The existence of responsiveness to stress, prior to 15 days of age, is indicated by significant elevations in serum corticosterone 15 minutes after saline injection, exogenous ACTH and exposure to ether at all ages studied (5, 7, 9, 11 and 13 days). The relatively low level of serum corticosterone, 15 minutes after ether, in the young rat is not due to a delayed stress response; this is indicated by the observation that 9 and 15 day old rats do not achieve adult corticosterone levels by up to 1 hour after a 1 minute lactation show a retardation of the maturation of the hypothalamo-hypophyseal-adrenal axis as indicated by a subnormal response to ether stress. This retardation is not observed in 15 day old offspring of mothers malnourished during pregnancy. This study of the influence of pre- and postnatal malnutrition will be extended to 10 as well as 20 and 25 day old pups to further assess the maturational delay. Thyroid feeding during pregnancy retards the development of stress responsiveness, whereas given during lactation it leads to its enhancement. Thyroid feeding during pregnancy followed by nutritional restriction during pregnancy, but not the reverse, severely retards the responsiveness to stress. Serum levels of thyroxine will be studied in these animals to determine the mechanism of this thyroid hormone influence (direct/hormonal vs. indirect/nutritional). The influence of malnutrition during pregnancy or lactation on the development of circadian corticosterone rhythm will be studied; furthermore, the influence of thyroid feeding in modifying this corticosterone rhythm of pre- and postnatally malnourished rats will also be examined.